Deficijencija B12 vitamina kod deteta majke na veganskoj ishrani

Vitamin B12 deficiency usually occurs in exclusively breastfed infants whose mothers have pernicious anaemia or are vegetarian. Early treatment of vitamin B12 deficiency in infants can prevent potentially neurologic sequelae. A male child aged 13 months has been hospitalized due to failure to thrive, feeding problems, pallor, weakness and hypotonia. During the pregnancy mother did not eat meat and during lactation she also excluded eggs and milk. The child was exclusively breastfed. Laboratory investigations showed a haemoglobin level of 3.5 g/dL, haematocrit 10%, red blood cell count of 0.99 × 1012/L, white blood cell count of 4.23 × 109 /L and platelet count of 55 × 109 /L. Vitamin B12 level was low. A bone marrow aspiration finding was consistent with megaloblastic anaemia. The magnetic resonance imaging showed brain atrophy. Vitamin B12 in a dose of 10µg per kg was applied intramuscularly daily for 2 weeks, then once weekly. Three days after initiating B12 vitamin therapy there was an improvement in the blood count with the gradual improvement of neurological state. Vitamin B12 deficiency is a treatable cause of pancytopenia and neurological dysfunction in children and should be considered as differential diagnosis in an infant with neurological symptoms.Deficijencija B12 vitamina se obično javlja kod odojčadi koja su na prirodnoj ishrani a čije majke imaju pernicioznu anemiju ili su vegetarijanci. Pravovremeno lečenje deficijencije B12 vitamina kod odojčadi može da prevenira potencijalne neurološke posledice. Malo muško dete uzrasta 13 meseci je hospitalizovano zbog nenapredovanja, problema sa hranjenjem, bledila, slabosti i hipotonije.Tokom trudnoće majka nije jela meso dok je tokom dojenja iz ishrane isključila i jaja i mleko. Dete je isključivo dojeno. U laboratorijskim nalazima nivo hemoglobina je iznosio 3,5 g/dl, hematokrit 10%, broj eritrocita je bio 0.99×1012/L, broj leukocita 4.23×109 /L i broj trombocita 55×109 /L. Nivo B12 vitamina je bio snižen. Nalaz biopsije kostne srži ukazivao je na megaloblastnu anemiju. Na magnetnoj rezonanci endokranijuma viđena je atrofija mozga. Vitamin B12 u dozi od 10 mikrograma/kg primenjen je intramuskularno svakodnevno tokom 2 nedelje, potom jednom nedeljno.Tri dana od započinjanja terapije zabeleženo je poboljšanje hematoloških vrednosti uz postepeno poboljšanje neurološkog statusa. Deficijencija B12 vitamina je uzrok pancitopenije i neurološke disfuncije kod dece koju je moguće lečiti. Kod odojčeta sa neurološkim simptomima ova deficijencija treba da bude razmotrena kao diferencijalna dijagnoza

Electrolytic D/H isotope separation efficiency and electrocatalytic activity of Mo-Pt intermetallic phases

The aim of this work was to investigate efficiency of the electrolytic separation of hydrogen isotopes (D/H), from alkaline 6 M KOH solution as standard electrolyte, on the Mo-Pt intermetallic phases as cathode materials. We measured the isotope separation factor (alpha) of the single-stage process, as a basic parameter determining the isotope separation efficiency. Furthermore, we have found that some combinations of activating compounds (ionic activators added directly into the electrolyte, assuming in situ activation) can reduce energy needs per mass unit of hydrogen produced, as well as the isotope separation efficiency, compared to those of the standard electrolyte. Also, the electrocatalytic ability of Mo-Pt intermetallic phases for the hydrogen evolution was investigated and evaluated at fixed over-potential (energy input) trough measured current density. Such investigations offer a possibility to optimize the electrolytic process, based on a significant upgrade of the efficiency regarding two needs: hydrogen production and isotope separation. (c) 2007 Elsevier B.V. All rights reserved

Influence of carvedilol on chronic renal failure progression in spontaneously hypertensive rats with adriamycin nephropathy

Background: In this study, the effects of carvedilol, antihypertensive (alpha-beta blocker) agent with antiproliferative and antioxidative properties, on slowing down of chronic renal failure (CRF) progression in spontaneously hypertensive rats (SHR) with adriamycin (ADR) nephropathy were examined. Methods: Eighty adult (24 weeks) SHR were divided into four groups: Control group: 20 SHR; ADR group: 20 SHR treated with ADR (2 mg/kg i.v. twice in 20 days); ADR-C group: 20 SHR treated with ADR and with carvedilol (30 mg/kg/day); ADR-CC group: 20 SHR treated with carvedilol and captopril (60 mg/kg/day). Systolic blood pressure was measured every two weeks, renal blood flow (RBF), mean arterial pressure (MAP) and renal vascular resistance (RVR) were determined at Weeks 6 and 12, creatinine clearance and proteinuria at Weeks -3 (see measurements), 6 and 12. The rats were sacrificed at Weeks 6 and 12 after the second ADR injection. Glomerular sclerosis, tubulointerstitial and blood vessel changes were determined by semiquantitative scoring. Results: Carvedilol decreased systolic blood pressure. It decreased RVR and MAP, and increased RBF significantly. Carvedilol also significantly decreased interstitial infiltration in the early phase of the study, slowed down the development of interstitial fibrosis and tubular atrophy and decreased blood vessel changes. The hemodynamic and morphological effects of carvedilol were associated with slowing down the CRF progression as well as a mild decrease in proteinuria. Captopril addition to carvedilol improved its effects especially on prevention of tubulointerstitial changes. Conclusions: Results of this experimental study showed beneficial effect of carvedilol and its combination with captopril on CRF progression, indicating that clinical Studies are warranted

Effect of carvedilol on pulse pressure and left ventricular hypertrophy in spontaneously hypertensive rats with adriamycin nephropathy

Recent studies indicated pulse pressure as a risk factor for left ventricular hypertrophy, myocardial infarction, congestive heart failure and stroke as well as chronic renal failure progression. The present study examined the effects of carvedilol and its combination with captopril on blood pressure, left ventricular hypertrophy, kidney vascular changes and kidney function in spontaneously hypertensive rats with adriamycin nephropathy. Four groups of 20 SHR each were involved: (1) control group: SHR; (2) ADR group: SHR treated with ADR (2 mg/kg i.v. twice in 20 days); (3) ADR-C group: SHR treated with ADR and carvedilol (30 mg/kg/day) and (4) ADR-CC group: SHR treated with ADR and carvedilol (30 mg/kg/day) and captopril (60 mg/kg/day). Systolic-, diastolic- and mean-pressures and pulse pressure were determined at weeks 6 and 12 after the second ADR injection; and body weight, creatinine clearance and proteinuria at weeks -3, 6 and 12. The rats were sacrificed at week 6 or 12, the weights of the left and right ventricles and kidneys measured and the kidney vascular index was calculated as described by Bader and Mayer. Both carvedilol alone and combined with captopril significantly reduced systemic blood pressure but the effect of the latter was more pronounced and registered from week 4 till the end of the study. Carvedilol and its combination with captopril significantly decreased SBP, DBP and MAP. They also decreased PP, prevented the development of LVH, and renal vascular changes and slowed the progression of chronic renal failure and these effects were stronger in the ADR-CC group than in the ADR-C group. The antihypertensive drugs failed to prevent proteinuria in ADR SHR. Significant positive correlations were found between PP (but not SBP, DBP and MAP) and both proteinuria and Ccr in all groups of rats. In conclusion, carvedilol alone, but more strongly in combination with captopril, significantly reduced blood pressure, PP, LVH, renal blood vessel changes and chronic renal failure progression

Finasteride Has Regionally Different Effects on Brain Oxidative Stress and Acetylcholinesterase Activity in Acute Thioacetamide-Induced Hepatic Encephalopathy in Rats.

Finasteride (FIN) inhibits neurosteroid synthesis and potentially improves the course of hepatic encephalopathy (HE). This study aimed to investigate the effects of FIN on brain oxidative stress and acetylcholinesterase (AchE) activity in acute thioacetamide-induced HE in rats. Male Wistar rats were divided into groups: 1. control; 2. thioacetamide-treated group (TAA; 900 mg/kg); 3. finasteride-treated group (FIN; 150 mg/kg); 4. group treated with FIN and TAA (FIN+TAA). Daily doses of FIN (50 mg/kg) and TAA (300 mg/kg) were administered intraperitoneally during three days and in FIN+TAA group FIN was administered 2h before every dose of TAA. FIN pretreatment prevented TAA-induced rise in malondialdehyde level in the cortex due to restoration of catalase activity and increased expression of superoxide dismutase 1 (SOD1) and induced an increase in malondialdehyde level in the thalamus due to reduction of glutathione peroxidase (GPx) and glutathione reductase (GR) activity. Although FIN pretreatment did not affect malondialdehyde level in hippocampus and caudate nucleus, hippocampal SOD1 expression was higher (p<0.05) and GR activity lower in FIN+TAA vs. TAA group (p<0.05). GPx activity was lower in caudate nucleus in FIN+TAA vs. TAA group (p<0.01). FIN pretreatment prevented TAA-induced rise in AchE activity in the thalamus and caudate nucleus and AchE activity correlates inversely in the thalamus (p<0.05) and positively in caudate nucleus (p<0.01) with malondialdehyde level. FIN has regionally selective effects on oxidative stress and AchE activity in the brain in acute TAA-induced HE in rats. The prooxidant role of FIN in the thalamus may be causally linked with inhibition of AchE

The effects of finasteride (FIN) and thioacetamide (TAA) on acetylcholinesterase (AchE) activity in various brain regions.

<p>The significance of the difference was estimated by ANOVA with Fisher’s <i>post hoc</i> test (*p<0.05 and **p<0.01 <i>vs</i>. control in the same region). For details see caption for Figs <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0134434#pone.0134434.g001" target="_blank">1</a> and <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0134434#pone.0134434.g002" target="_blank">2</a>.</p

The effects of finasteride (FIN) and thioacetamide (TAA) on (a) malondialdehyde (MDA) level and (b) superoxide dismutase (SOD) activity in various brain regions.

<p>Four brain regions (dorsolateral frontal cortex, hippocampus, thalamus and caudate nucleus) were isolated 24 h after administration of the last dose of TAA and crude synaptosomal fractions were prepared for determination of parameters of oxidative stress. The significance of the difference was estimated by ANOVA with Fisher’s <i>post hoc</i> test (*p<0.05 and **p<0.01 <i>vs</i>. control in the same region). For details see caption for <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0134434#pone.0134434.g001" target="_blank">Fig 1</a>.</p

The effects of finasteride (FIN) and thioacetamide (TAA) on (a) reduced glutathione (GSH) level, (b) glutathione peroxidase (GPx), (c) glutathione reductase (GR) and (d) catalase activity in various brain regions.

<p>The significance of the difference was estimated by ANOVA with Fisher’s <i>post hoc</i> test (*p<0.05 and **p<0.01 <i>vs</i>. control, #p<0.05 and ##p<0.01 <i>vs</i>. TAA group in the same region). For details see caption for Figs <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0134434#pone.0134434.g001" target="_blank">1</a> and <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0134434#pone.0134434.g002" target="_blank">2</a>.</p